Pulseless Electrical Activity

Introduction

Pulseless electrical activity (PEA), also known as electromechanical dissociation, is a clinical condition characterized by unresponsiveness and impalpable pulse in the presence of sufficient electrical discharge. A lack of ventricular impulse often points to the absence of ventricular contraction, but the opposite is not always true. It means that the electrical activity is a pertinent, but not sufficient, condition for contraction. In case of cardiac arrest, the organized ventricular electrical activity does not usually follow sufficient ventricular response. The word “sufficient” is being used to describe a degree of ventricular mechanical activity that is adequate to generate a palpable pulse.

Pulseless electrical activity does not necessarily mean the lack of mechanical activity. There can be ventricular contractions and detectable pressures in the aorta which are also known as pseudo-PEA. True pulseless electrical activity is a state in which cardiac contractions are lacking in the presence of coordinated electrical impulses. Pulseless electrical activity can include a number of organized cardiac rhythms that may be supraventricular in origin (sinus versus nonsinus) or ventricular in origin (accelerated idioventricular or escape). An impalpable pulse should not always be taken as a pulseless electrical activity because it may be due to severe peripheral vascular abnormality. [1][2][3]

Etiology

The etiology of pulseless electrical activity is classified into primary/cardiac and secondary/noncardiac causes.

Primary pulseless electrical activity, often caused by or related to cardiac arrest is due to depletion of myocardial energy reserves. It responds poorly to therapy. [4][5][6]

Causes of secondary pulseless electrical activity include the famous "5 Hs and 5 Ts." These are as follows:

5 Hs

Hypovolemia

Hypoxia

Hydrogen ion (acidosis)

Hypo/hyperkalemia

Hypothermia

5 Ts

Tension pneumothorax

Trauma

Tamponade

Thrombosis, pulmonary

Thrombosis, coronary

Epidemiology

The incidence of pulseless electrical activity is different among different United States patient populations. It accounts for approximately 20% of sudden cardiac deaths outside of the hospital setting.[7][8]

A study found that 68% of the recorded in-hospital deaths and 10% of all in-hospital deaths were attributed to pulseless electrical activity. In addition, the hospitalized patients are more likely to suffer from pulmonary embolism among other complications. Pulseless electrical activity is the first documented rhythm in 30 to 38% of adults with in-hospital cardiac arrest.

Beta blockers and calcium channel blockers may alter contractility, leading to increased susceptibility and resistance to treatment.

Females are more likely to develop pulseless electrical activity as compared to the male population. The risk of pulseless electrical activity increases over the age of 70, especially in the female population.

Pathophysiology

Pulseless electrical activity occurs when an insult involving CVS, GIT, or the respiratory system results in the inability of the cardiac muscle to generate adequate force in response to electrical depolarization. This adverse event decreases cardiac contractility, and the situation gets severe by potential acidosis, hypoxia, and worsening vagal tone. More compromise of the inotropic state of the cardiac muscle leads to insufficient mechanical activity, despite the presence of electrical activity. It causes degeneration of cardiac rhythm, and eventually, death follows.

Transient coronary occlusion usually does not cause pulseless electrical activity unless hypotension or other arrhythmias are involved. Respiratory failure leading to hypoxia is one of the most common causes of pulseless electrical activity, responsible for about half of the PEA cases. The following are other mechanisms for pulseless electrical activity:

Decreased preload

Increased afterload

Decreased contractility

Decreased cardiac contractility has been related to changes in intracellular calcium levels, which explains why patients with beta blockers or calcium channel blockers are more prone to developing pulseless electrical activity and may become unresponsive to therapy.[9][10][11]

History and Physical

A thorough yet quick history should be reviewed while paying special attention to the following:

Risk factors for myocardial infarction or pulmonary embolism

Any trauma

Severe fluid loss

Exposure to low temperatures

Risk of metabolic derangements

Physical findings, as the name indicates, include an absence of palpable pulses in the foremost finding.

Drugs used include epinephrine and atropine. Epinephrine should be administered in 1 mg doses intravenously/intraosseously (IV/IO) every 3 to 5 minutes during pulseless electrical activity arrest. Higher doses of epinephrine have not shown to improve survival or neurologic outcomes in most patients. Selected patients, like those with beta blockers or calcium channel blockers overdose, may benefit from higher-dose epinephrine.

If the detected rhythm is bradycardia that is associated with hypotension, then atropine (1 mg IV q3-5 min, up to three doses) should be administered. This is considered the optimal dose, beyond which no further benefit will occur. Note that atropine may cause pupillary dilation; therefore, this sign cannot be used to assess neurologic function.

NaHCO3 may be used only in patients with severe, systemic acidosis, hyperkalemia, or tricarboxylic acid overdose. The dose is 1 mEq/kg. Avoid routine administration of sodium bicarbonate as it worsens intracellular and intracerebral acidosis without affecting mortality.

Pericardial drainage and emergent surgery may be lifesaving in appropriate patients with pulseless electrical activity. In a patient with a refractory case and chest trauma, a thoracotomy may be performed.

Near pulseless electrical activity or a very low-output state may also be managed with the circulatory assistance (e.g., intra-aortic balloon pump, extracorporeal membrane oxygenation, cardiopulmonary bypass, and ventricular assist device).

Differential Diagnosis

Accelerated idioventricular rhythm

Acidosis

Cardiac tamponade

Drug overdose

Hypokalemia

Hypothermia

Hypovolemia

Hypoxemia

Myocardial ischemia

Pulmonary embolism

Syncope

Tension pneumothorax

Ventricular fibrillation

Prognosis

Patients who have sudden cardiac arrest due to pulseless electrical activity also have a poor outcome. In one study of 150 such patients, 23% were resuscitated and survived to hospital admission; only 11% survived until hospital discharge.

Consultations

After the patient has been stabilized, consultation can be sought from the respective departments. For example, one may call for a surgery consult if a large pulmonary embolus is detected or from toxicology/IM in cases of drug overdoses or poisoning.

Pearls and Other Issues

Pulseless electrical activity is a major cause of mortality, especially in hospitalized, elderly patients.

Immediate evaluation to look for cause is warranted.

Good quality CPR is the first thing needed after the activation of the emergency response system.

Epinephrine and atropine can be used in conjunction with CPR.

The foremost priority is the hemodynamic stability of the patient

Enhancing Healthcare Team Outcomes

All healthcare workers, especially emergency department physicians, nurses, urgent care workers, internists, intensivists and trauma specialists who look after patients must be certified in ATLS. While there are many causes of cardiac arrest, one needs to be aware of puleseless electrical activity, which carries a high mortality rate.

The first step in managing pulseless electrical activity is to start chest compressions according to ACLS protocol along with using epinephrine, while simultaneously looking for any reversible causes. Once a diagnosis is made, begin immediate management i.e., decompression of pneumothorax, pericardial drain for tamponade, fluids infusion, correction of body temperature, administration of thrombolytics, or surgical embolectomy for pulmonary embolus.